Prkcd, encoding Protein kinase C delta, is a member of the PKC family. It has various biological properties and is involved in multiple biological processes. It plays a role in immune tolerance, effector functions against pathogens, and is associated with pathways related to cell activation, cytokine production, and mitophagy [2,3,6].

Prkcd deficiency, a rare genetic disorder, has been identified as a monogenic cause of systemic lupus erythematosus. The phenotypic variability in patients with Prkcd deficiency delineates its broad and critical role in immune tolerance and effector functions [2]. In chronic obstructive pulmonary disease (COPD), Prkcd contributes to the development of the disease by promoting inflammatory response, apoptosis, mitochondrial dysfunction, and MUC5AC hypersecretion, suggesting it could be a potential therapeutic target [1]. In gastric cancer, TRIM69 suppresses anoikis resistance and metastasis through ubiquitin-proteasome-mediated degradation of Prkcd [4]. In triple negative breast cancer (TNBC), PRKCD_pY313 activates Src and p38 MAPK to promote TNBC progression [5]. Also, in the Chinese Han population, polymorphisms in Prkcd are associated with Vogt-Koyanagi-Harada disease susceptibility [6].

In conclusion, Prkcd is crucial in various biological functions including immune-related processes and cell-signaling pathways. Its role in diseases such as systemic lupus erythematosus, COPD, gastric cancer, TNBC, and Vogt-Koyanagi-Harada disease has been revealed through functional studies. Understanding Prkcd's functions in these disease areas may provide new insights for potential therapeutic strategies.